Small Intestine

Foundations

Anatomy, Physiology, and Pathophysiology

There are several different types of SBO. The term mechanical obstruction implies the presence of a physical barrier to the movement of the intestinal contents. Obstructions of this type can be further sub-classified according to the cause of the obstruction relative to the intestinal wall ( Box 78.1 ). Lesions external to the intestinal tract cause obstruction by compressing the gut. This is most commonly the result of post-operative adhesions, though hernias and intra-peritoneal neoplasms may also cause external obstruction. Lesions intrinsic to the intestinal wall itself can also cause mechanical obstruction, such as primary intestinal neoplasms, localized infection (e.g., intestinal wall tuberculosis), or trauma (e.g., a hematoma of the intestinal wall). Finally, lesions within the intestinal lumen can lead to obstruction, such as bezoars, ingested foreign bodies, or gallstone ileus.

BOX 78.1

Lesions Causing Small Bowel Obstruction Relative to the Intestinal Wall

External to Intestinal Wall

• Postoperative adhesions

• Hernias

• Volvulus

• Compressing masses (tumors, abscesses, hematomas)

Intrinsic to Intestinal Wall

• Primary neoplasms

• Inflammatory (e.g., Crohn disease, radiation enteritis)

• Infectious causes (e.g., intestinal tuberculosis)

• Intussusception

• Traumatic (intestinal wall hematoma)

• Intraluminal

• Bezoars

• Foreign bodies

• Gallstones

• Ascaris infestation

Another important distinction of SBO is whether the obstruction is a simple or closed loop obstruction. A simple obstruction occurs at a single point. A closed loop–type obstruction involves obstruction at two locations, thus creating a segment of bowel with compromised blood flow proximally and distally. Closed loop obstructions are seen when a twist develops in the mesentery or, in the case of an internal hernia, when a loop of bowel becomes entrapped in a defect in the mesentery ( Fig. 78.1 ). If not promptly recognized and relieved, a closed loop obstruction can quickly lead to intestinal infarction and necrosis, which has twice the mortality rate of simple small bowel obstruction.

In contrast to a mechanical obstruction, a neurogenic or functional obstruction occurs as a result of disruption of the normal coordinated peristaltic activity of the gastrointestinal (GI) tract in the absence of a physical blockage within the intestinal lumen, leading to dysfunction in the enteric propulsion. This is also commonly referred to as an adynamic ileus. The causes of adynamic ileus are listed in Box 78.2 . It often occurs in patients who have undergone abdominal surgery and is usually transient in nature. Some degree of functional obstruction is considered normal after surgery and results from multiple factors, including an inflammatory response to intestinal manipulation, the release of several hormones and neurotransmitters triggered by surgery, and the effects of opioid analgesics. In addition to surgery, a number of medical conditions can lead to a functional SBO, including infection or metabolic abnormalities, particularly hypokalemia.

BOX 78.2

Causes of Adynamic Ileus

• Metabolic disease (especially hypokalemia)

• Medications (e.g., narcotics)

• Infection (retroperitoneal, pelvic, intrathoracic)

• Abdominal trauma

• Laparotomy

The term pseudo-obstruction refers to a poorly understood and complex syndrome in which the signs and symptoms of mechanical obstruction, including the appearance of dilated bowel on radiography, are present in the absence of a mechanical lesion. This is thought to involve disruption of intestinal pacemaker activity controlled by a specialized group of cells found in the GI tract called the interstitial cells of Cajal. These cells regulate the contractility of the intestinal smooth muscle and are under the influence of the enteric nervous and autonomic systems. Pathology at any one of these sites can lead to pseudo-obstruction. Causes include degenerative neuropathies, autoimmune or paraneoplastic disease including systemic lupus erythematosus, or scleroderma, as well as hereditary conditions. The symptoms of pseudo-obstruction are often chronic and respond poorly to treatment.

Pathophysiology

Regardless of the etiology, with the development of an SBO the interruption of normal flow through the intestinal lumen triggers a cascade of physiologic changes that correlate with the progressive development of symptoms. In a mechanical obstruction, the bowel proximal to the blockage first becomes mildly dilated through the accumulation of partially digested food and normal intestinal secretions. These secretions are referred to as succus entericus and are secreted by cells lining the intestinal wall in response to mechanical stimulation. Increased intestinal dilation causes an increase in peristalsis throughout the intestines, which can trigger frequent and loose bowel movements early in the progression of the obstruction as well as episodes of nausea or vomiting. As the process continues, the bowel wall becomes edematous and the normal absorptive function of the intestinal wall decreases, leading to further accumulation of contents in the intestinal lumen proximal to the obstruction. Owing to the loss of normal intestinal motility, bacterial overgrowth begins to occur in the proximal small bowel. It is this overgrowth in a location of the intestines that is normally relatively sterile that explains the feculent nature of the emesis observed in patients with SBO. As the obstruction continues, there is a transudative fluid loss into the peritoneal cavity, leading to worsening hypovolemia and dehydration. In addition, if the obstruction is proximal in location, continued bouts of emesis can lead to electrolyte abnormalities, metabolic alkalosis, severe hypovolemia, or shock.

In a closed loop obstruction, the escalation in intraluminal pressure occurs much more rapidly as the intestinal contents cannot flow retrograde. Intestinal venous congestion and then arterial obstruction can also progress quickly to intestinal ischemia and infarction, referred to as a strangulation obstruction. If not promptly relieved, necrosis and intestinal perforation can occur. The resulting leakage of the intestinal contents into the peritoneum can lead to peritonitis and sepsis.

In the developed world, the most common cause of SBO is post-operative adhesions, which account for approximately 60% of cases ( Fig. 78.2 ). A large meta-analysis estimated the overall incidence of adhesive SBO following abdominal surgery at 2%. These adhesions develop as a result of a process involving the interaction among numerous types of cells, cytokines, and coagulation factors caused by damage to the peritoneal surfaces, with a subsequent increase in fibrin formation. Operations on the small intestine, colon, appendix and uterus appear to have a higher risk of adhesion formation than procedures in the upper abdomen involving the gallbladder, stomach or pancreas. Emergency surgery also appears to be a risk factor compared to elective procedures. Over the last several years, numerous physical bio-absorbable barriers and pharmacologic agents have been evaluated as potentially useful in decreasing the formation of post-operative adhesions with mixed results. Although they appear to minimize the formation of postoperative adhesions, they have not been shown to improve clinical outcomes.

The second most common cause of SBO is tumors, which are responsible for roughly 20% of cases. This includes malignancies, such as adenocarcinomas, carcinoid tumors, lymphomas, or sarcomas, as well as benign conditions, including adenomas, leiomyomas, or lipomas. In addition to these primary GI tumors, gynecologic cancers, especially ovarian cancer, are a common cause of SBO. Metastatic disease is yet another tumor-related cause of SBO, including metastatic breast, skin, or testicular cancer.

Hernias are the third most common cause of SBO, found in approximately 10% of cases. Similar to their relative frequency in general, ventral and inguinal hernias are usually encountered, but femoral, parastomal, lateral ventral (also called spigelian hernia ), and internal hernias may also lead to SBO. Although rare in the general population, internal hernias are a recognized complication of bariatric surgery, especially when a Roux-en-Y type procedure has been performed. In this group, internal hernias have been described in up to 5% of patients and usually develop at the mesocolic window. Another rare type of hernia is the obturator hernia. This hernia develops into the obturator foramen and is especially common in older women who have recently lost a significant amount of weight. The female pelvis is wider and the obturator canal is more oblique in women than in men. This, in combination with a loss of preperitoneal fat in older, often emaciated patients, predisposes to the development of an obturator hernia. Because an external mass is absent, the diagnosis can be especially challenging, which explains why it carries the highest mortality of any abdominal hernia, nearly 70%, when it is incarcerated.

Gallstone ileus is a rare but important cause of mechanical SBO ( Fig. 78.3 ). It is responsible for 1% to 4% of all cases of mechanical obstruction and is most frequently seen in older adults with underlying medical problems. The pathogenesis involves the entry of a gallstone into the intestinal tract through a biliary-enteric fistula. This arises from the localized inflammation of cholecystitis and, in most cases, entry occurs via a cholecystoduodenal fistula. After entering the intestinal lumen, the gallstone migrates distally. As a stone moves through the intestinal lumen, it often increases in size as bowel content sedimentation becomes attached. Eventually, the gallstone becomes lodged, usually in the ileum, which is the narrowest segment of the small bowel, and the patient then develops symptoms of obstruction.

Small bowel volvulus occurs infrequently but is a potentially catastrophic cause of SBO. This condition results from the abnormal twisting of a loop of small bowel around the axis of its own mesentery. Although it accounts for only 3% to 6% of SBO cases in the West, it is much more common in Africa, India, and the Middle East, where it is responsible for up to 20% of cases. Primary small bowel volvulus occurs in an otherwise normal abdominal cavity; secondary small bowel volvulus occurs when a congenital or acquired abnormality leads to the development of the volvulus.

A reported increase in primary small bowel volvulus during Ramadan has been attributed to eating a large amount of food bulk after prolonged fasting, causing the proximal jejunum to descend into the pelvis, displacing empty small bowel loops upward and initiating malrotation. Alterations in gut motility and increased small bowel length have also been suggested as possible predisposing factors.

Causes of secondary small bowel volvulus include intestinal malrotation caused by the arrest of normal rotation of the embryonic gut, or post-operative adhesions. In the case of congenital malrotation, more than 50% of affected children present for evaluation before 1 month of age with small bowel volvulus. Because a small bowel volvulus is a classic closed loop obstruction, prompt recognition and surgical treatment are imperative because the risk of strangulation is high.

The term intussusception describes the invagination or “telescoping” of a part of the small intestine into itself. This results in the development of venous and lymphatic congestion, with consequent intestinal edema, which can lead to intestinal ischemia and perforation. Intussusception occurs in patients of all ages but is most frequently seen in children younger than 2 years. It is the most common cause of intestinal obstruction in infants 6 to 36 months of age. Unlike ileocolic intussusception, which can often be treated nonoperatively by enema reduction, surgery is more often required in cases of intussusception limited only to the small bowel. In children, the cause is usually idiopathic, but several studies have shown an association with adenovirus infection. It has been postulated that enteric adenovirus infection may trigger stimulation of the lymphatic tissue in the intestinal tract, which may create a lead point for the intestine to be dragged into itself by the normal peristaltic activity of the intestines. In contrast to the idiopathic nature of intussusception in children, a mechanical cause is found in more than 90% of adult cases. Tumors, benign or malignant, are discovered as the initiating cause in more than 65% of adult cases. Adult intussusception has been reported in association with acquired immunodeficiency syndrome (AIDS) as a result of lymphoma or unusual infections, such as atypical mycobacterial infections.

Clinical Features

Differential Diagnosis

The diagnosis of SBO should be considered in any patient with abdominal pain and vomiting, especially if there is a history of prior abdominal surgery. It may be difficult to differentiate SBO from nonobstructive intestinal motility disorders, such as adynamic ileus or intestinal pseudo-obstruction, by history and examination alone.

Other conditions to consider include gastroenteritis, mesenteric adenitis, constipation, cholelithiasis or nephrolithiasis, ectopic pregnancy, pancreatitis, peptic ulcer disease, atypical myocardial infarction, leaking abdominal aortic aneurysm (AAA), or mesenteric ischemia. These pathologies have typical signs, symptoms, and diagnostic findings that can help differentiate them from one another and from SBO, but this may be challenging, especially early in the course of illness.

Diagnostic Testing